Although the N-type Ca2+ channel plays a role in a variety of neuronal functions, N-type Ca2+ channel alpha1B-deficient mice exhibit normal life span without apparent behavioral or histologic abnormalities. To examine whether the reason for their normal behavior is compensation by other Cav2 channel alpha1 or beta subunit genes and to analyze whether genetic background influences the subunit expression pattern, we studied the alpha1A, alpha1E, beta1b, beta2, beta3 and beta4 subunit mRNA levels in cerebellum of alpha1B-deficient mice with CBA x C57BL/6 or CBA/JN background. In cerebellum of the mice with a CBA x C57BL/6 background, alpha1A mRNA was expressed at a higher level than that in wild-type or heterozygous mice, but difference in the expression levels of alpha1E, beta1b, beta2, beta3 and beta4 subunits was not found among wild-type, heterozygous, and homozygous mice. In cerebellum of alpha1B-deficient mice with CBA/JN background, beta4 mRNA was expressed at a higher level than that in wild-type or heterozygous mice, but alpha1A, alpha1E, beta1b, alpha2, beta3 and transcripts were expressed at similar levels in all genotypes. Therefore, a possible explanation of the normal behavior of alpha1B-deficient mice is that Cav2 channel family members compensate for the deficiency, and that the change of functional subunit expression pattern for compensation differs in animals with different genetic backgrounds.